Developmental problems associated with folic acid deficiency are well known in the art. Perhaps neural tube defects in fetuses are the most common problem associated with folate deficiency. Expecting mothers are routinely placed on a folic acid regimen. Additionally, nursing mothers are also supplemented with folic acid to continue to provide nutrition to the newborn. During the prenatal and perinatal periods, folate is essential for adequate enclosure of the neural tube by dermal tissues. In recent studies, it has been shown that women with increased levels of plasma homocysteine and decreased levels of erythrocyte folate have a greater risk of having an offspring with a neural tube defect. It is believed that during the early stages of pregnancy (prior to the development of the placenta) transport of folates to the fetus is primarily performed by the maternal erythrocytes. Inadequate folate levels in maternal erythrocytes are a significant factor in the lack of progression of neural tube closure in utero.
Folate helps produce and maintain new cells; this is critically important in cells with rapid growth that undergo frequent cell division such as in infancy and pregnancy. Folate is needed to form DNA and RNA, and both adults and children need folate to make normal red blood cells. It is essential that folates are part of the daily nutritional consumption for adequate human health.
Folates also play a critical role in the reduction of plasma homocysteine levels. An increased amount of homocysteine in the plasma has been associated with heart disease. Folates have been shown to reduce the calcification of plaques during an acute ischemic attack; thereby reducing the long-term effects of cardiovascular disease. Thus, folates are major components of cardiovascular functionality.
Folate is an essential water-soluble B. vitamin that occurs naturally in food. As a result of these important metabolic activities, several dietary derivatives of folate are manufactured as supplements. Although most of the derivatives are capable of becoming converted into the metabolically active form (6S) 5-methyltetrahydrofolate, the enzyme kinetics of such conversion can differ dramatically as well as the absorption rate and it is these differences that are important in determining the hierarchy of performance.
Folates are a group of pteroyglutamate acids that become structurally and functionally altered when reduced (adding electrons) or oxidized (removing electrons). In humans, folates are absorbed most readily as 5-methyltetrahydrofolate and it is the principal circulating form of folate. Other derivatives are hydrolyzed in the intestinal jejunum and the liver to the active form with an intermediate stable form (5,10-methylenetetrahydrofolate).
5-methyltetrahydrofolate is the predominant form of folate in the circulatory system and is the type of folate that can cross the blood-brain barrier. 5-methyltetrahydrofolate is critical for brain development and normal mental health.
The endocrine system is a system of glands, each of which secretes a type of hormone into the bloodstream to regulate the body. The endocrine system is an information signal system like the nervous system. Hormones regulate many functions of an organism, including mood, growth and development, tissue function, and metabolism.
Thyroid-related medical conditions, and medications that are used in connection with thyroid conditions, are known to cause hematological issues in individuals, as well as in fetuses of such individuals who may be pregnant, or the children who receive breast milk from such individuals who have thyroid-related medical conditions and/or who are on thyroid medication. In addition, these thyroid-related medical conditions, and the medications that are used in connection with thyroid conditions, are known to cause adverse hepatic conditions regarding the liver, as well as having an adverse impact on other organs. Moreover, in addition to those persons who have thyroid-related medical conditions or who are taking medications for thyroid conditions, environmental conditions, and environmental contaminants are also known to impact the thyroid system of an individual, as well as the fetus of such individual or child nursing from such individual. Thus, the thyroid system can be impacted by thyroid-related medical conditions that develop within one's own body, by certain medications, and by the environment.
Typically, thyroid conditions are treated with medication to address the thyroid condition and bring the patient to a euthyroid state. That is the focus of the medical community and pharmaceutical community. However, bringing an individual to a euthyroid state does not sufficiently address the adverse conditions associated with low folate, as well as vitamin B12, and specifically low cerebrospinal folate. The medical and pharmaceutical communities have not been able to sufficiently address the further complications the thyroid-related medical conditions, and/or the medications that are used in connection with thyroid conditions, cause. For instance, anti-thyroid drugs are known to cause (a) numerous blood disorders (including, but not limited to, megaloblastic anemia, pancytopenia, aplastic anemia, neutropenia, agranulocytosis, thrombocytopenia, and leukopenia), (b) bone marrow suppression, and (c) hepatic dysfunction. In addition, thyroid-related medical conditions are known to cause similar conditions. For instance, hypothyroidism is known to cause iron, folate and/or vitamin B12 deficiencies, which with respect to folate or vitamin B12 deficiencies, can cause “macrocytic” or “megaloblastic” hematological conditions leading, in some cases, to bone marrow suppression and hepatic dysfunction, as well as dysfunction in other organs (polyglandular failure syndrome for instance).
Even further, autoimmune conditions like chronic autoimmune thyroiditis and Hashimoto's thyroiditis associated with pernicious anemia can cause even further vitamin B12 deficiencies that will not be corrected solely by thyroid hormone replacement, but also require specific vitamin B12 supplementation. Moreover, additional conditions that complicate the clinical picture are (1) “masked megaloblastic anemia” conditions that can arise from simultaneous iron and folate/vitamin B12 deficiencies, (2) lack of vitamin B12 which is critical in the metabolic pathway of converting folate into its biologically useful form, and (3) “polymorphisms” that are commonplace. For instance, the methylenetetrahydrofolate (MTHFR) polymorphism is very common, by some accounts up to 40% of the U.S. population. As a result, some individuals are naturally more susceptible to having cerebrospinal folate issues, or ancillary folate and/or vitamin B12 issues, than others based on whether or not they have the polymorphism. Yet, notwithstanding the foregoing, thyroid-related medical conditions and drugs that are used to treat thyroid conditions are not augmented with suitable folate and B12 supplementation protocols sufficient to prevent or ameliorate the adverse effects of low cerebrospinal folate.